Paper Information

Title: 

INVESTIGATING THE EFFECT OF LPS ON NEUROTOXICITY AND APOPTOSIS IN PC12 NEURONAL CELLS: ROLE OF BAX AND BCL2

Type: POSTER
Author(s): FOTOVAT ESKANDARI N.A.H.*,SHARIFI A.M.,AMIR MOZAFARI N.
 
 *DEPARTMENT OF PHARMACOLOGY AND CELLULAR AND MOLECULAR RESEARCH CENTER, SCHOOL OF MEDICINE, IRAN UNIVERSITY OF MEDICAL SCIENCES, TEHRAN, IRAN
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2009Volume 19
 
 
Abstract: 

Bacterial lipopolysaccharides (LPS) are human pathogens. Gram-negative bacteria and their endotoxins may be a causal or complicating factor in many serious diseases. The syndromes most commonly connected with bacterial endotoxins are sepsis and septic shock, which are systemic complications of many diseases. Whatever the source, exposure to endotoxin induces a systemic inflammatory response that involves many interconnected cellular and plasma mediators. Among the many disorders induced by LPS, neurodegenerative diseases such as Parkinson are reported and are of great interest. Despite the evidences on LPS-induced neurodegeneration, the exact mechanism is unknown.
This study, therefore, is sought to examine the neurotoxicity effect of LPS on the PC12 cells, an in-vitro model system to study viability of neuronal cells. The cell viability was evaluated by MTT assy. The expression of proapoptotic Bax and anti-apoptotic Bcl2 were measured by immunobloting. The results showed that LPS in 2oo μg/ml concentration, significantly reduced cell viability after 72 hrs. In Western blot analysis, the ratio of Bax/Bcl-2 protein expression in cells treated with LPS was significantly increased compared to controls.From the present results, it might be concluded that LPS can cause PC12 cell death, in which apoptosis plays an important role possibly by the mitochondrial pathway through higher expression of Bax proapoptotic protein.

 
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